Homo sapiens strain:A549
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA229764 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR1046682.fastq.gz | Fastqsanger.gz | |||
| SRR1046682_1.fastq.gz | Fastqsanger.gz | |||
| SRR1046682_2.fastq.gz | Fastqsanger.gz | |||
| SRR1046363.fastq.gz | Fastqsanger.gz | |||
| SRR1046363_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 50 |
Similar Datasets
Project description:Analysis of viral and host RNA populations in the context of in vitro paramyxovirus infection.
| PRJNA222426 | ENA
Project description:Analysis of viral and host RNA populations in the context of in vitro paramyxovirus infection.
| PRJNA222427 | ENA
Project description:Analysis of viral and host RNA populations in the context of in vitro paramyxovirus infection.
| PRJNA221641 | ENA
Project description:Newcastle disease virus (NDV) is an avian paramyxovirus that causes major economic losses to the poultry industry around the world, with NDV pathogenicity varying due to strain virulence differences. However, the impact of intracellular viral replication and the heterogeneity of host responses among cell types are unknown. Here, we investigated the heterogeneity of lung tissue cells in response to NDV infection in vivo and that of chicken embryo fibroblast cell line DF-1 to NDV infection in vitro using single-cell RNA sequencing.
2022-12-31 | GSE202128 | GEO
Project description:Many events in viral infection are regulated through post-translational modification. In the case of positive-sense RNA viruses such as SARS-CoV-2 which encodes two viral proteases, proteolytic cleavage of both viral and cellular proteins is crucial for productive viral infection. In this work we study proteolysis in the context of SARS-CoV-2 infection of ACE2-A549 and Vero E6 cells, infected at a multiplicity of infection of 1, with samples harvested at 0,6,12 and 24h post-infection. Neo-N-termini and lysine residues were labelled at the protein level with TMTpro reagents prior to tryptic digestion. For unenriched samples, the trypsin-digested material was then fractionated offline, and analysed by LC-MS/MS for the study of total protein abundance over the infection timecourse. For enriched samples, unblocked neo-N-termini generated by tryptic digested were labelled with undecanal and depleted, yielding a sample enriched for blocked neo-N-termini (TMTpro, N-terminal acetylation, and pyroGlu). The enriched samples were similarly fractionated offline and analysed by LC-MS/MS. Please note this is one of several linked datasets. This dataset contains data from ACE2-A549 cells infected with SARS-CoV-2, prior to enrichment.
2021-07-29 | PXD021145 | Pride
Project description:This study investigates the modulatory effects of baricitinib on the host immune response to Rift Valley Fever Virus (RVFV) infection. A549 cells and organoids were treated with 5 µM baricitinib or vehicle control prior to infection with recombinant RVFV (rRVFV) or mock treatment. Total RNA was isolated at 8 and 24 hours post-infection, and mRNA was enriched for transcriptome sequencing. We performed RNA-seq analysis to identify differentially expressed genes and pathways affected by baricitinib treatment during RVFV infection, providing insights into potential therapeutic mechanisms of JAK inhibition in viral infections.
2025-03-28 | GSE292720 | GEO
Project description:Many events in viral infection are regulated through post-translational modification. In the case of positive-sense RNA viruses such as SARS-CoV-2 which encodes two viral proteases, proteolytic cleavage of both viral and cellular proteins is crucial for productive viral infection. In this work we study proteolysis in the context of SARS-CoV-2 infection of ACE2-A549 and Vero E6 cells, infected at a multiplicity of infection of 1, with samples harvested at 0,6,12 and 24h post-infection. Neo-N-termini and lysine residues were labelled at the protein level with TMTpro reagents prior to tryptic digestion. For unenriched samples, the trypsin-digested material was then fractionated offline, and analysed by LC-MS/MS for the study of total protein abundance over the infection timecourse. For enriched samples, unblocked neo-N-termini generated by tryptic digested were labelled with undecanal and depleted, yielding a sample enriched for blocked neo-N-termini (TMTpro, N-terminal acetylation, and pyroGlu). The enriched samples were similarly fractionated offline and analysed by LC-MS/MS. Please note this is one of several linked datasets. This dataset contains data from ACE2-A549 cells infected with SARS-CoV-2, enriched for neo-N-termini.
2021-07-29 | PXD021152 | Pride
Project description:Viral infection has a great impact on cellular expression profile of non-coding RNAs and genes. By microarray screening, our study identified 79 long non-coding RNAs (lncRNAs) and 140 mRNAs that were differentially expressed in human lung epithelial A549 cells infected with Zika virus (ZIKV). The bioinformatics analysis indicated that many differentially expressed lncRNAs were located in same chromosome as the differentially expressed mRNAs; and these lncRNAs and mRNAs were involved in the host responses to viral infection, including the innate immune response.
2018-12-20 | GSE124094 | GEO
Project description:Viral infection is usually studied at the population level by averaging over millions of cells. However, infection at the single-cell level is highly heterogeneous, where most infected cells give rise to none or few viral progeny while some cells produce thousands. Analysis of HSV-1 infection by population averaged measurements has taught us a lot about the course of viral infection, but has also produced contradictory results, such as the concurrent activation and inhibition of type I interferon signaling during infection. Here, we combine live-cell imaging and single-cell RNA sequencing to characterize viral and host transcriptional heterogeneity during HSV-1 infection of primary human cells. We find extreme variability in the level of viral gene expression among individually infected cells and show that they cluster into transcriptionally distinct sub-populations. We find that anti-viral signaling is initiated in a rare group of abortively infected cells, while highly infected cells undergo cellular reprogramming to an embryonic-like transcriptional state. This reprogramming includes the re-localization of b-catenin into the host nucleus and viral replication compartments and is required for late viral gene expression and progeny production. These findings uncover the transcriptional differences in cells with variable infection outcomes and shed new light on the manipulation of host pathways by HSV-1.
2019-04-26 | GSE126042 | GEO
Project description:Paramyxoviruses are negative sense single-stranded RNA viruses that comprise many important human and animal pathogens, including human parainfluenza viruses. These viruses bud from the plasma membrane of infected cells after the viral ribonucleoprotein complex (vRNP) is transported from the cytoplasm to the cell membrane via Rab11a marked recycling endosomes. The viral proteins that are critical for mediating this important initial step in viral assembly are unknown. Here we use the model paramyxovirus, murine parainfluenza virus 1, or Sendai virus (SeV), to investigate the roles of viral proteins in Rab11a-driven virion assembly. We previously reported that infection with SeV containing high levels of copy-back defective viral genomes (DVGs) generates heterogenous populations of cells, with cells enriched in full-length virus producing viral particles containing standard or defective viral genomes, while cells enriched in DVGs did not, despite high levels of defective viral genome replication. Here we take advantage of this heterogenous cell phenotype to identify proteins that mediate interaction of vRNPs with Rab11a. We examine the role of matrix protein and nucleoprotein and determine that they are not sufficient to drive interaction of vRNPs and recycling endosomes. Then, using a combination of mass spectrometry and comparative protein abundance and localization in DVG- and FL-high cells, we identify viral polymerase complex components L and, specifically, its cofactor C proteins as interactors with Rab11a. We find that accumulation of these proteins within the cell is the defining feature that differentiates cells that proceed to viral egress from cells which remain in replication phases. Paramyxoviruses are a family of viruses that include a number of pathogens with significant burdens on human health. Particularly, human parainfluenza viruses are an important cause of pneumonia and bronchiolitis in children and do not have any vaccines or direct acting antivirals. These cytoplasmic replicating viruses bud from the plasma membrane and coopt cellular endosomal recycling pathways to traffic viral ribonucleoprotein complexes from the cytoplasm to the membrane of infected cells, yet the viral proteins required for viral engagement with the recycling endosome pathway is not known. Here we use the model paramyxovirus Sendai virus, or murine parainfluenza virus 1, to investigate the role of viral proteins in this initial step in viral assembly. We find that viral polymerase components large protein L and accessory C proteins are necessary for engagement with recycling endosomes. These findings are important in identifying viral targets for the development of antivirals.
2020-08-06 | PXD019637 | Pride